. Author manuscript; available in PMC: 2008 Jul 12.

Published in final edited form as: Exp Biol Med (Maywood). 2008 Apr 29;233(7):860–873. doi: 10.3181/0801-RM-12

Table 1.

Host SPARC regulates metastasis

		Metastatic Incidence (%)						Metastatic Events
Genotype	Cell Type	n=	Lymph	Peritoneal	Liver	Other	Total	Lymph	Peritoneal	Liver	Other	Total
WT	PRV	6	16.7	66.7	16.7	0	66.7	1	10	1	0	12
*SPARC ^-/-*	PRV	6	66.7	83.3	0	33.3	83.3	14	34 ^{at, bt}	0	1	49^{at, bt}
WT	MMP9	5	20.0	60.0	0	20.0	80.0	1	4	0	1	6
*SPARC ^-/-*	MMP9	6	33.3	16.7	0	0	50.0	5	4	0	0	9

The influence of host SPARC and tumor-derived MMP9 on metastasis rate was evaluated after orthotopic implantation of pancreatic PAN02 tumors in WT and SPARC^-/- mice. The total metastatic events and metastatic incidence in specific target organs was determined in one experiment at the time of sacrifice by visual inspection of each organ with a dissection scope under illumination with blue light to excite GFP in the tumor cells (n=number of animals in each group). Metastatic incidence is displayed as the percentage (%) of animals/group with a metastatic lesion in the target organ. The incidence of metastasis was compared between treatment groups were using a Tukey-type multiple comparison test for proportions (42). Statistical significance was set at 5%. Metastatic events are displayed as the total number of metastatic lesion in the target organ for the group. The number of metastatic events per mouse per organ were compared to median events per organ for the sample population using a Tukey-type multiple comparison test for medians (42). Trends (p<0.10) detected are indicated by ^at, vs. WT MMP9; ^bt, vs. SPARC MMP9.